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Hierarchy of resistance to cervical neoplasia mediated by combinations of killer immunoglobulin-like receptor and human leukocyte antigen loci

  1. Author:
    Carrington, M.
    Wang, S.
    Martin, M. P.
    Gao, X. J.
    Schiffman, M.
    Cheng, J.
    Herrero, R.
    Rodriguez, A. C.
    Kurman, R.
    Mortel, R.
    Schwartz, P.
    Glass, A.
    Hildesheim, A.

  2. Author Address

    Sci Applicat Int Corp, Natl Canc Inst, Lab Genom Divers, Basic Res Program, Ft Detrick, MD 21702 USA. NCI, Div Canc Epidemiol & Genet, Hormonal & Reprod Epidemiol Branch, Bethesda, MD 20892 USA. Proyecto Epidemiol Guanacaste, San Jose 3016151, Costa Rica. Johns Hopkins Med Inst, Div Gynecol Pathol, Baltimore, MD 21231 USA. Penn State Univ, Milton S Hershey Med Ctr, Hershey, PA 17033 USA. Yale Univ, Sch Med, New Haven, CT 06520 USA. Kaiser Permanente Ctr Hlth Res, Portland, OR 97227 USA Carrington, M, Sci Applicat Int Corp, Natl Canc Inst, Lab Genom Divers, Basic Res Program, Ft Detrick, MD 21702 USA
    1. Year: 2005
    2. Date: APR 4
  2. Journal: Journal of Experimental Medicine
    1. 201
    2. 7
    3. Pages: 1069-1075
  4. Type of Article: Article
  1. Abstract:

    Killer immunoglobulin-like receptor (KIR) recognition of specific human histocompatibility leukocyte antigen (HLA) class I allotypes contributes to the array of receptor-ligand interactions that determine natural killer (NK) cell response to its target. Contrasting genetic effects of KIR/HLA combinations have been observed in infectious and autoimmune diseases, where genotypes associated with NK cell activation seem to be protective or to confer susceptibility, respectively. We show here that combinations of KIR and HLA loci also affect the risk of developing cervical neoplasia. Specific inhibitory KIR/HLA ligand pairs decrease the risk of developing neoplasia, whereas the presence of the activating receptor KIR3DS1 results in increased risk of disease, particularly when the protective inhibitory combinations are missing. These data suggest a continuum of resistance conferred by NK cell inhibition to susceptibility involving NK cell activation in the development of cervical neoplasia and underscore the pervasive influence of KIR/HLA genetic variation in human disease pathogenesis

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External Sources

  1. View record in Web of Science®
  2. WOS: 000228187300008

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